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Chapter 25 : Bloodstream Infections

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Abstract:

Bloodstream infections (BSIs) and sepsis rank among the top reasons for human mortality for hospitalized patients. The full breadth of sepsis syndromes are particularly dangerous to any immunocompromised patient. Sepsis is one of the oldest of medical syndromes and dates back to the time in which Hippocrates characterized it as a clinical syndrome ( ). Worldwide estimates of sepsis prevalence exceed 19 million cases per year, with over 750,000 in the United States ( ). While only 2% of patients are admitted to the hospital with severe sepsis, they represent at least 10% of all ICU admissions in the U.S. ( ).

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016
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Figures

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Figure 1

The host response in severe sepsis. The host response to sepsis is characterized by both proinflammatory responses (top of panel, in red) and anti-inflammatory immunosuppressive responses (bottom of panel, in blue). The direction, extent, and duration of these reactions are determined by both host factors (e.g., genetic characteristics, age, coexisting illnesses, and medications) and pathogen factors (e.g., microbial load and virulence). Inflammatory responses are initiated by interaction between pathogen-associated molecular patterns expressed by pathogens and pattern-recognition receptors expressed by host cells at the cell surface (toll-like receptors [TLRs] and C-type lectin receptors [CLRs]), in the endosome (TLRs) or in the cytoplasm (retinoic acid inducible gene 1-like receptors [RLRs] and nucleotide-binding oligomerization domain-like receptors [NLRs]). The consequence of exaggerated inflammation is collateral tissue damage and necrotic cell death, which results in the release of damage-associated molecular patterns, so-called danger molecules that perpetuate inflammation at least in part by acting on the same pattern-recognition receptors that are triggered by pathogens. Reprinted from reference ( ), with permission.

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016
Permissions and Reprints Request Permissions
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Image of Figure 2
Figure 2

Organ failure in severe sepsis and dysfunction of the vascular endothelium and mitochondria. Sepsis is associated with microvascular thrombosis caused by concurrent activation of coagulation (mediated by tissue factor) and impairment of anticoagulant mechanisms as a consequence of reduced activity of endogenous anticoagulant pathways (mediated by activated protein C, antithrombin, and tissue factor pathway inhibitor), plus impaired fibrinolysis owing to enhanced release of plasminogen activator inhibitor type 1 (PAI-1). The capacity to generate activated protein C is impaired at least in part by reduced expression of two endothelial receptors: thrombomodulin (TM) and the endothelial protein C receptor. Thrombus formation is further facilitated by neutrophil extracellular traps (NETs) released from dying neutrophils. Thrombus formation results in tissue hypoperfusion, which is aggravated by vasodilatation, hypotension, and reduced red-cell deformability. Tissue oxygenation is further impaired by the loss of barrier function of the endothelium owing to a loss of function of vascular endothelial (VE) cadherin, alterations in endothelial cell-to-cell tight junctions, high levels of angiopoietin 2, and a disturbed balance between sphingosine-1 phosphate receptor 1 (S1P1) and S1P3 within the vascular wall, which is at least in part due to preferential induction of S1P3 through protease-activated receptor 1 (PAR1) as a result of a reduced ratio of activated protein C to thrombin. Oxygen use is impaired at the subcellular level because of damage to mitochondria from oxidative stress. Reprinted from reference ( ), with permission.

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of Figure 3
Figure 3

Algorithms for diagnosis, prognostication, and prediction of response to therapy. FA = fluorescent antibody stain; AFB = acid-fast bacilli; mAFB = modified AFB; SSTI = skin and soft tissue infection; LDT = Laboratory developed test.

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016
Permissions and Reprints Request Permissions
Download as Powerpoint

References

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Tables

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Table 1

Summary of interesting reviews and publications related to viral and miscellaneous pathogen bloodstream infections

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016
Generic image for table
Table 2

Predisposing factors that contribute to immunosuppression

Citation: Martinez R, Wolk D. 2016. Bloodstream Infections, p 653-689. In Hayden R, Wolk D, Carroll K, Tang Y (ed),

Diagnostic Microbiology of the Immunocompromised Host, Second Edition

. ASM Press, Washington, DC. doi: 10.1128/microbiolspec.DMIH2-0031-2016

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